Actual evidence for neuromonitoring-guided intensive care following severe traumatic brain injury

Abstract

Therapeutic interventions following severe traumatic brain injury (TBI) are substantially influenced by complex and interwoven pathophysiological cascades involving both, local and systemic alterations. Our main duty is to prevent secondary progression of the primary damage. This, in turn, obliges us to actively search and identify secondary insults related, for example, to hypoxia, hypotension, uncontrolled hyperventilation, anaemia, and hypoglycaemia. During pharmacological coma we must rely on specific cerebral monitoring which is indispensable in unmasking otherwise occult changes. In addition, extended neuromonitoring (SjvO2, ptiO2, microdialysis, transcranial Doppler sonography, electrophysiological studies, direct brain perfusion measurement) can be used to define individual pathological ICP levels which, in turn, will support our decision making. Extended neuromonitoring expands the limited knowledge derived from ICP and CPP values, thereby allowing us to adequately adapt the type, extent and speed of different therapeutic interventions. A more individualised and flexible treatment concept depends on extended neuromonitoring. The present review addresses current evidence in favour of extended neuromonitoring used to guide treatment options aimed at improving intensive care treatment of patients with severe TBI. With increasing experience gained by the use of extended neuromonitoring in clinical routine we may expect that the evidence obtained within the individual patient will translate to convincing evidence on a larger scale for the entire study population.

Interrelationship between blood and tissue lactate in a general intensive care unit: A subcutaneous adipose tissue microdialysis study on 162 critically ill patients

“…Microdialysis is widely used in neurointensive care [7][8][9][10], having great potential for exploring the pathophysiology of brain injury. Importantly, continuous monitoring of extracellular metabolites provides early warning of impending cerebral hypoxia/ischemia before neurologic deterioration, allowing timely implementation of neuroprotective therapies [11,12].…”

Changes in plasma phenylalanine, isoleucine, leucine, and valine are associated with significant changes in intracranial pressure and jugular venous oxygen saturation in patients with severe traumatic brain injury

“…This, in turn, could facilitate metabolic impairment reflected e.g., by decreased SjvO 2 and result in sustained edema formation unmasked e.g., by increased ICP. Whether TBI patients also show an imbalance between AAA and BCAA and if changes in plasma AAA and BCAA concentrations are possibly associated with increased cerebral oxygen consumption and elevated ICP, thereby expanding contemporary neuromonitoring (Stover 2011) has not been investigated yet.…”

Implementation of cerebral microdialysis at a community-based hospital: A 5-year retrospective analysis

“…Figures 6 and 7 provide some examples of how MD data helped in our treatment paradigm in these specific cases. However, because the information and implications from cerebral MD and multimodal brain monitoring are rapidly evolving,[2331] it is difficult to recommend a protocolized approach to the use of cerebral MD data at this time. All of the information including clinical status and radiographic findings must be taken into consideration.…”